Parkinsonism

[LeslieV.Barns]

Thank goodness, a place where I might actually learn something....but I wish Ray Peat would put his fine mind to the problem (that seems to be increasing in incidence, including more people of all ages) of the various motor and non-motor problems that get lumped together under the Parkinson's label. Now they tell me they're not sure I even have it. The usual rules of diet don't seem to apply because the neurotransmitters are already out of whack, and then the pharmaceuticals make things worse.

I am taking about 1,000 mg. of levo-carb a day, and the docs have put me on an SSRI (citalopram) to help me withdraw from clonazepam, then they put me on lorazepam to replace the clonazepam, while I was still in withdrawal (my own initiative) from taking a 'Z' drug for sleep then going off it far too fast. It seems all my neurotransmitters are out of whack, and the usual dietary advice doesn't help. Protein blocks levo-carb, sugary sweets make the serotonin skyrocket, I've got histamine coming out all over, and I don't think there is a GABA receptor in my body that still works.
Anybody got any ideas where to start? My goal is to get off the citalopram and lorazepam, then tackle the levo-carb, and if necessary, try the mucuna bean.

 

[tara]

Leslie

I don't know much about parkinsonism, or about the relevant neurotransmitter systems. Peat has mentioned it, though mostly tangentially, in a number of his articles - have you seen them? If you go to type parkinson into the search box on his articles page you'll find several: http://raypeat.com/articles/

Withdrawing and recovering from drug use can get complicated. I notice that lisuride is sometimes prescribed for it, and Peat has has been relatively favourable things about lisuride, I think motly for it's anti-serotonin effects. I don't know how that would relate to interctions with the other drugs you mention, though.
He also favours coffee for many situations, and I think there may also be some mainstream research showing coffee to be helpful against parkinsonism?

I don't know how much you've read of or about Peat's ideas, but a lot revolves aroound maintaining good general cellular energy production as generally protective of many systems, including neurological systems. So there is a lot of focus on getting and keeping metabolism high, and providing good nourishment is an important part of that. Also on trying to avoid spending too much time in catabolic stress states, so that the body has a better chance to repair itself rather than just keep getting run down. Many issues have better chance of sorting themselves out or at least slowing right down if given good conditions.

Have you had a go at implementing any of Peat's diet ideas?
Have you had a go at figuring out how your geneal energy metabolism is running - eg by monitoring temperatures and pulse and/or thyroid hormone labs?

Are you saying you've been advised to keep protein low? Does sugar cause seotonin to rise for you even when it is accompanied by all the other nutrients needed to make good use of it, like the potassium and magnesium etc in oj, and b-vits, etc? What about if you eat/drink it in small frequent meals to help keep blood sugars more stable?

Whatever other tactics make sense for you, minimising dietary polyunsaturated oils is one of the first steps many of us here take, because there are so many ways thet can mess with the system. Hopefully you wil be able to find a way to get in all the nutrition you need to repair and maintain, even with current constraints, but it looks as though this is going to be a challenge for you.

Peat has talked about progesterone being neuroprotective. You could read his articles about the benefits of progesterone (and the damage caused by estrogen), if you haven't already.

If you are not in a position to get lots of sunlight on your skin everyday, I wonder whether supplementary red light could be a useful tactic for you.

Hopefully there will be ohters here who know more. Otherwise, I think it would be interesting to ask him advice directly.

Good luck

 

[LeslieV.Barns]

Thanks so much for your reply,

I have just started trying to apply some of Ray Peat's dietary advice and am thankful that he is around. I have just finished reading Pharmageddon by David Healy, a British psycho-pharmacologist, who just excoriates the drug companies (and doctors) for the damage they are doing to thousands (?millions) of people, both adults and often now, children too, with their dangerous drugs and wrong-headed 'science'.
thanks again.

 

[aguilaroja]

...I have just started trying to apply some of Ray Peat's dietary advice....

As Tara mentions, Dr. Peat's website, raypeat.com, has a search function where some references to Parkinson's can be found. If less familiar, you might review some of the Peat-y basics, discussed at Dr. Peat's site, in his books, here and elsewhere. For instance, pregnenolone has wide neuro-protective functions. Reading Dr. Peat's view about other brain decline situations, such as Alzheimer's, may give a general framework.
http://raypeat.com/articles/articles/th ... ones.shtml

Probably in the testing so far, basic thyroid blood tests have been done. It would be good to review the numbers with a Peat-y lens. In addition to other general supportive metabolic factors, there are interesting fairly recent studies about the usefulness of thiamine and also taurine in PD situations. Thiamine and taurine have specific threads in this forum as well.

There's basis for suspecting that Levodopa/Carbidopa preparations deplete pyridoxal-5-phosphate (P5P/"activated" vitamin B6). In one situation familiar to me, augmenting P5P noticeably helped Levodopa/Carbidopa effectiveness.
http://www.dovepress.com/the-parkinson3 ... ticle-CPAA

Time permitting, I'll mention more thoughts at a later date.

http://raypeat.com/articles/articles/hy ... dism.shtml

"A disease or its treatment can obscure the presence of hypothyroidism. Parkinson's disease is a clear example of this. (Garcia-Moreno and Chacon, 2002: “... in the same way hypothyroidism can simulate Parkinson's disease, the latter can also conceal hypothyroidism.”)"

http://raypeat.com/articles/articles/iron-dangers.shtml

"Excess iron's role in infectious diseases is now well established, and many recent studies show that it is involved in degenerative brain diseases, such as Parkinson's, ALS (Lou Gehrig's disease), Huntington's chorea, and Alzheimer's disease. Iron is now believed to have a role in skin aging, atherosclerosis, and cataracts of the lenses of the eyes, largely through its formation of the 'age pigment.'"

http://raypeat.com/articles/articles/se ... sion.shtml

"In Parkinson’s disease, the benefits seen from increasing the concentration of dopamine could result from dopamine’s antagonism to serotonin; anti-serotonin drugs can alleviate the symptoms, and 5-hydroxytryptophan can worsen the symptoms (Chase, et al., 1976). Other movement disorders, including akathisia and chorea, can be produced by serotonin. In autism, repetitive motions are a common symptom, and serotonin is high in the blood serum and platelets of autistic children and their relatives. Irritable bowel syndrome, another kind of “movement disorder,” can be treated effectively with anti-serotonin agents. This syndrome is very common in women, with premenstrual exacerbations, when estrogen is highest. One of the side effects of oral contraceptives is chorea, uncontrollable dancing movements. Some research has found increased serotonin in people with Huntington’s chorea (Kish, et al., 1987), and positive results with bromocriptine have been reported (Agnoli, et al., 1977).
The neurosteroid, allopregnanolone, for which progesterone is the precursor, facilitates the inhibitory action of GABA, which is known to be deficient in some disorders of mood and movement. This suggests that progesterone will be therapeutic in the movement disorders, as it is in various mood problems. Progesterone has some specific antiserotonin actions (e.g., Wu, et al., 2000)."

BMJ Case Rep. 2013 Aug 28;2013. pii: bcr2013009289. doi: 10.1136/bcr-2013-009289.
High-dose thiamine as initial treatment for Parkinson's disease.
Costantini A1, Pala MI, Compagnoni L, Colangeli M.

Parkinson's disease (PD) is a systemic disease with motor and non-motor deficits. We recruited three patients with newly diagnosed PD. They were not under anti-Parkinson's therapy. Plasmatic thiamine was within healthy reference range. We performed the Unified Parkinson's Disease Rating Scale (UPDRS) and started a parenteral therapy with high doses of thiamine. The therapy led to a considerable improvement in the motor part of the UPDRS ranging from 31.3% to 77.3%. From this clinical observation, it is reasonable to infer that a focal, severe thiamine deficiency due to a dysfunction of thiamine metabolism could cause a selective neuronal damage in the centres that are typically hit in this disease. Injection of high doses of thiamine was effective in reversing the symptoms, suggesting that the abnormalities in thiamine-dependent processes could be overcome by diffusion-mediated transport at supranormal thiamine concentrations.
PMID: 23986125
---
J Neurol Sci. 2012 May 15;316(1-2):1-8. doi: 10.1016/j.jns.2012.02.008. Epub 2012 Mar 2.
Thiamine and Parkinson's disease.
Lu'o'ng Kv1, Nguyên LT.

Parkinson's disease (PD) is the second most common form of neurodegeneration in the elderly population. PD is clinically characterized by tremors, rigidity, slowness of movement and postural imbalance. A significant association has been demonstrated between PD and low levels of thiamine in the serum, which suggests that elevated thiamine levels might provide protection against PD. Genetic studies have helped identify a number of factors that link thiamine to PD pathology, including the DJ-1 gene, excitatory amino acid transporters (EAATs), the α-ketoglutarate dehydrogenase complex (KGDHC), coenzyme Q10 (CoQ10 or ubiquinone), lipoamide dehydrogenase (LAD), chromosome 7, transcription factor p53, the renin-angiotensin system (RAS), heme oxygenase-1 (HO-1), and poly(ADP-ribose) polymerase-1 gene (PARP-1). Thiamine has also been implicated in PD through its effects on L-type voltage-sensitive calcium channels (L-VSCC), matrix metalloproteinases (MMPs), prostaglandins (PGs), cyclooxygenase-2 (COX-2), reactive oxygen species (ROS), and nitric oxide synthase (NOS). Recent studies highlight a possible relationship between thiamine and PD. Genetic studies provide opportunities to determine which proteins may link thiamine to PD pathology. Thiamine can also act through a number of non-genomic mechanisms that include protein expression, oxidative stress, inflammation, and cellular metabolism. Further studies are needed to determine the benefits of using thiamine as a treatment for PD.
PMID: 22385680

http://www.ncbi.nlm.nih.gov/pubmed/22903433
Amino Acids. 2014 Jan;46(1):31-46. doi: 10.1007/s00726-012-1382-z. Epub 2012 Aug 19.
Taurine and central nervous system disorders.
Menzie J1, Pan C, Prentice H, Wu JY.

In the present era, investigators seek to find therapeutic interventions that are multifaceted in their mode of action. Such targets provide the most advantageous routes for addressing the multiplicity of pathophysiological avenues that lead to neuronal dysfunction and death observed in neurological disorders and neurodegenerative diseases. Taurine, an endogenous amino acid, exhibits a plethora of physiological functions in the central nervous system. In this review, we describe the mode of action of taurine and its clinical application in the neurological diseases: Alzheimer's disease, Parkinson's disease and Huntington's disease.

"It has been reported that there is age-related decline of taurine which correlated strongly with striatal dopamine loss (Dawson et al. 1999) and that there is a lower level of taurine in patients with PD than in control patients (Molina et al. 1997). This suggests that, similar to AD, the loss of taurine in PD could swing the scale towards neuronal degeneration. On the other hand, a report by Navneet et al. (2008) found that taurine was not protective against dopaminergic neuronal loss in a MPP? animal model. They reported the dose of taurine (250 mg/kg, i.p.) used was similar to another study (Mankovskaya et al. 2000) that showed neuroprotection. Such conflict could arise from the difference in experimental paradigms and war- rants more research in animal models of PD."

 

[BingDing]

Welcome to the forum!

I took a look at http://davidhealy.org/books/pharmageddo ... a-tragedy/. Many people here reject the authoritarian status of doctors and basically decide for themselves what is best. That book is ample reason why.

I am somewhat simplistic. Tyrosine -> L-Dopa -> dopamine is the metabolic pathway, I have seen some improvements in ease of movement supplementing 1g of tyrosine first thing in the morning.

The abstract above calls taurine an endogenous AA but it is often considered conditionally essential, that is we need to get it from diet in some conditions. The brain has large amounts of taurine but it doesn't readily cross the blood brain barrier so has to be synthesized. Supplementing taurine might spare it in the body and improve brain levels (totally my theory, RP has never said that).

Glycine and taurine are inhibitory and are seen as broadly beneficial. But using isolated AAs is not 100% safe (per RP) so using them with a protein meal might be better (again my theory, not RPs).

I'm also a big fan of getting replete in micronutrients, probably because I wasn't for some 50+ years. Magnesium and vitamin D deficiencies are widespread and the trace minerals are important. There are lots of threads about the best forms, especially vitamins K and E. Multi-vitamins are probably not sufficient.

I could ramble on for quite awhile but I'll just say you have a very good chance of getting healthy with Peat's advice. It is definitely worth the time to understand it all.

 

[NathanK]

I am with you. My mother has Parkinson's and it runs in my family. I've only recently started to connect the dots that I could develop the dopamine centric disorder as I age (I'm 38). Parkinson's, RLS, bruxism, anxiety, and running on adrenaline in general are all in the dopamine metabolism pathway, which is how I know. I hope to improve my current condition and avert any future problems. I wish you the best of luck on your journey.